Adrenocortical response to hypertonic saline in rats with lateral hypothalamic lesions.

Used plasma corticosterone levels to assess the response to stress induced by ip injections of hypertonic saline in 27 male albino Harlan-Sprague rats with lateral hypothalamic (LH) or sham lesions. Ss with LH lesions displayed a corticosterone response equal to that of normal Ss under basal conditions, after control injections of isotonic saline, and 20 min after injection of hypertonic saline (1.5 M, 1.0 ml/100 g of body weight). The corticosterone response of Ss with LH lesions, however, was significantly less than that of normal Ss 90 min after injection of hypertonic saline when no water was available. With access to water, normal Ss displayed substantial drinking (14.5 ml/90 min), which resulted in a reduction in plasma corticosterone concentrations to a level observed after a control injection of isotonic saline, but the little water ingested by Ss with LH lesions (2.5 ml) had no effect on the pituitary-adrenal system. It is concluded that the failure of Ss with LH lesions to drink following a hydrational challenge is not the result of an exaggerated response to stress. (17 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of lateral hypothalamic lesions on food intake of rats during exposure to cold.

Two experiments investigated the feeding behavior of 41 male Sprague-Dawley rats with lateral hypothalamic (LH) lesions and 13 Ss with chemical lesions of central dopaminergic neurons. LH damage impaired both physiological and behavioral responses of Ss during exposure to a 5°C environment. The LH-lesioned Ss usually did not conserve heat in the cold as well as did controls (n?=?13), nor did they always increase their caloric intake to meet their energy needs. However, when given sucrose solution to drink instead of water, LH-lesioned Ss increased their ingestion of chow in response to cold exposure. It is likely that the elevated consumption of palatable fluid served to relieve dehydration and thereby removed its constraints on eating, thus permitting hyperphagia to occur. In contrast to these results, Ss with large dopamine-depleting brain lesions, produced by intraventricular 6-hydroxydopamine treatments, always increased food intake when exposed to cold stress and demonstrated no apparent problems in peripheral vasoconstriction. Thus, it is unlikely that striatal dopamine depletions account for either the impaired feeding response or the inadequate heat conservation of rats with lateral hypothalamic lesions during cold stress. (33 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Acute homeostatic imbalances reinstate sensorimotor dysfunctions in rats with lateral hypothalamic lesions.

It has previously been demonstrated that rats recovered from aphagia and adipsia after large bilateral electrolytic lesions of the lateral hypothalamic (LH) area do not show the normal feeding response to 2-deoxyglucose or drinking response to polyethylene glycol. The present work found that such homeostatic imbalances reinstate the profound sensorimotor impairments that are seen in the immediate postoperative period but abate in parallel with the gradual recovery of ingestive behaviors. Administration of alpha methyltyrosine or spiroperidol produced sensory and motor dysfunctions in male albino Sprague-Dawley rats with LH lesions that were similar to those observed after 2-deoxyglucose. Results suggest that the residual feeding and drinking deficits of Ss with LH lesions after apparent recovery of function do not reflect specific loss of putative gluco- and volume-regulatory contributions to ingestive behavior. Instead, they indicate continued impairments in nonspecific activational components of motivation that normally are mediated, in part, by central dopaminergic neurons. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Active regulation to be lean by rats with ventromedial hypothalamic lesions.

52 adult female Long-Evans rats with electrolytic or radio-frequency thermocoagulatory lesions of the ventromedial hypothalamus (VMH) lived on pellet fragments or powdered chow containing as much as 1.2% quinine sulfate or lived in Skinner boxes with 45-mg pellets delivered contingent on FRs of leverpressing up to FR 128. Body weights maintained by VMH Ss were determined by the percentage of quinine in or the contingency of reinforcement of the food on which they lived. Even when Ss lived on highly adulterated or response-contingent food and were lean, they ate more of that food when the ambient temperature was reduced and less of that food during several weeks of forced feeding of eggnog. Weight maintenance in the cold and caloric compensation during forced feeding were as precise for VMH Ss eating highly adulterated chow or Noyes pellets contingent on high FRs as for VMH Ss eating laboratory chow ad lib, even though the former Ss at the time maintained weights no greater than intact Ss and the latter Ss were grossly obese. Regulation in the cold or during forced feeding was only a little less precise for Ss with lesions than for intact Ss. It may be as characteristic of VMH Ss that they eat to become lean and remain lean as that they eat to be obese. (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Drinking by rats after lateral hypothalamic lesions: A new look at the lateral hypothalamic syndrome.

Rats that have recovered from aphagia and adipsia following lateral hypothalamic lesions are believed to be incapable of experiencing thirst and drink water simply to facilitate the consumption of dry food. However, the present results from adult Sprague-Dawley albino rats indicate that these Ss will drink in response to dehydration of the intracellular or intravascular fluid compartments and to hyperangiotensinemia, if testing continues beyond a few hours. Comparable effects also were obtained in Ss with mesencephalic brain damage, which appeared to destroy portions of the substantia nigra and the ascending nigrostriatal dopaminergic projections. These findings, when placed in the context of a recent neurochemical model for recovery of function, suggest a new interpretation of the lateral hypothalamic syndrome. (2 p ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of lateral hypothalamic lesions and vagotomy on meal patterns in rats.

Studied meal patterns with liquid diets in 4 female Carworth CFE albino rats with lateral hypothalamic (LH) lesions and in 4 Ss with sham lesions, both before and after vagotomy. LH Ss reduced total intake following lesions but showed no differences from controls after vagotomy on measures of total daily intake, mean meal size, and frequency of feeding. Identical frequency distributions of meal sizes and intermeal interval durations were found in LH and control Ss after vagotomy. However, although sham-lesioned Ss showed significant positive correlations between meal size and subsequent intermeal-interval durations in all phases of the experiment, the LH Ss showed no such correlation following vagotomy. Thus, indices of microregulatory controls may be more sensitive in indicating feeding deficits. (25 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Body weight and gastric acid secretion in rats with subdiaphragmatic vagotomy and lateral hypothalamic lesions.

Investigated the role of the vagus in the lateral hypothalamic (LH) syndrome to body weight loss in 80 male Sprague-Dawley albino rats. Ss were divided into 4 groups: (a) Ss with bilateral LH lesions that were subsequently given a bilateral subdiaphragmatic vagotomy, (b) LH Ss that received a control vagotomy operation, (c) nonlesion Ss that were given a subdiaphragmatic vagotomy, and (d) nonlesion Ss that received a control vagotomy operation. Both LH lesions and vagotomy reduced body weight levels, though the effects differed in terms of the length of time required to reach initial maximal loss, the time required to reach chronic levels of maintenance, and the severity of body weight reduction. Fasting gastric acid secretion was lowered by LH lesions, and the extent of this reduction was positively correlated with the reduction in body weight. Gastric contents after a 24-hr fast were greater in vagotomized than in nonvagotomized Ss. These data are discussed in relation to the role of the vagus in maintaining body weight levels and in relation to the changes in gastric functioning after LH lesions and vagotomy. (42 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Failure of recovered lateral hypothalamic rats to learn specific food aversions.

Assigned 16 female Sprague-Dawley albino rats to either a group receiving lesions of the lateral hypothalamus, a group receiving lesions of the ventromedial nuclei of the hypothalamus, or a control group. After lesioned Ss recovered the ability to feed voluntarily, Ss were exposed to a procedure in which intake of a preferred diet was followed by LiCl poisoning. Whereas unoperated controls decreased subsequent intake of this diet and showed an aversion to it on a later preference test, most lesioned Ss showed little or no sign of having learned to avoid the poison-paired food. There was evidence, however, that the ability of brain-damaged Ss to learn this avoidance recovers over time. In Exp. II, intake of another preferred diet was accompanied by shock to the tongue. Again, lesioned Ss, unlike unoperated controls, appeared unable to associate ingestion of the diet with its aversive consequences. (35 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

CCK-8 inhibits ingestive behavior in rats with lateral hypothalamic 6-OHDA lesions

Male rats were injected with 6-hydroxydopamine in the lateral hypothalamus and tested for ingestive behavior starting on the day after the injection. The rats did not eat food pellets but readily ingested an intraorally infused nutritive solution. If given three daily intraoral infusions, 6-hydroxydopamine-treated rats defended their body weight and were as sensitive to the inhibitory effect of cholecystokinin octapeptide on intake as controls. Dopamine was reduced by 94% in the dorsal striatum five days after the 6-hydroxydopamine injection. Noradrenaline and serotonin were less markedly affected. Thus, while appetitive ingestive behavior is disrupted, consummatory ingestive behavior and body weight regulatory competence are only marginally affected by massive damage to forebrain dopamine neural networks.     

Circadian rhythms and partial recovery of regulatory drinking in rats after lateral hypothalamic lesions.

Eight sighted male albino rats that had recovered spontaneous ingestive behavior after lesions of the lateral hypothalamus were challenged with acute injections of hypertonic NaCl administered at different times during the day-night cycle. Nine intact controls were also studied. Following these injections, drinking was observed only during the nighttime. After morning injections Ss frequently waited until nightfall before drinking, whereas Ss injected at night showed much shorter delays in the behavioral response; a similar nocturnal predominance of drinking was seen after food deprivation and in the ad-lib situation. Studies in 6 blind lesioned Ss suggest that these effects were due to an endogenous circadian rhythm. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Increased motivation in rats with ventromedial hypothalamic lesions.

25 female albino rats were implanted with chronic electrodes aimed for the ventromedial hypothalamic area (VMH), deprived to 82% of normal weight, and trained on a 2-min VI schedule for food reinforcement. After rates of response became stable, bilateral DC lesions were made, and weight was held constant. Over 10 days after lesioning, Ss with extensive VMH damage showed increases in rates of response for food. Unilateral lateral hypothalamic lesions resulted in decreases in response rates followed by recovery, regardless of VMH damage. Under more severe deprivation (48 hrs and 72 hrs), Ss with extensive VMH damage showed further increases in response rate. Results indicate that VMH lesions increased food motivation. Some factors which can produce opposite results are discussed. (38 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Ontogeny of meal patterning in rats and its recapitulation during recovery from lateral hypothalamic lesions.

Investigated the development of feeding patterns in weanling rats and in rats with lateral hypothalamic lesions. 2 experiments were conducted with a total of 39 male albino Sprague-Dawley rats. From 16 to 25 days of age, the weanlings demonstrated a preprandial intake pattern (i.e., a positive correlation between meal size and time since the preceding meal). This subsequently declined while the postprandial relationship (correlation with time until subsequent meal) such that by 30-35 days of age a full adult pattern was observed. Ss recovering from lateral hypothalamic lesions, for a brief period, also demonstrated a preprandial intake pattern. The postprandial relationship was abolished by the lesion. Results suggest that the development of adult meal patterning results from maturation of lateral hypothalamic mechanisms governing meal initiation. (40 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Decrease in food intake following cortical spreading depression in static obese rats with ventromedial hypothalamic lesions.

Subjected 19 male and 23 female rats with ventromedial hypothalamic (VMH) lesions or with sham lesions to cortical spreading depression (CSD) 150 days after lesioning. Lesioned Ss showed a significantly lower food intake (as percentage of intake before CSD) than sham-lesioned Ss in the 14 days after CSD, but water intake did not differ between lesioned and sham-lesioned Ss. Both groups showed a slight decline in body weight, but lesioned Ss lost significantly more weight than sham-lesioned Ss. After 14 days, body weight, food intake, and water intake had returned to pre-CSD levels in both groups. Findings indicate that Ss with VMH damage are more sensitive to the effects of CSD than are normals and suggest that CSD acts to increase the activity of the VMH and to inhibit food intake, and this increase in activity is prolonged in VMH-lesioned Ss. (22 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of lateral hypothalamic lesions on placentophagia in virgin, primiparous, and multiparous rats.

Produced lesions of the lateral hypothalamus (LH) in 25 pregnant and 25 nonpregnant Sprague-Dawley rats through chronically implanted electrodes to investigate the effect of LH damage on placentophagia. Other variables investigated were prior parturitional experience and stimulus properties of the placenta. Lesions were produced under either anesthesia 24 hr prior to parturition in pregnant Ss and 24 hr prior to placenta presentation in nonpregnant Ss. Lesions produced aphagia to a liquid diet. Pregnancy was not a significant variable in the initiation of placentophagia, but prior parturitional experience was critical. Virgin and primiparous Ss did not exhibit placentophagia following LH damage, but multiparous Ss would eat placenta whenever the opportunity arose, independently of LH damage and pregnancy. (18 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Chonically reduced body weight in rats sustaining lesions of the lateral hypothalamus and maintained on palatable diets and drinking solutions.

12 male Holtzman rats sustaining lateral hypothalamic (LH) lesions regulated their body weight at a reduced level when maintained for 1 mo postlesion upon a wet mash diet. Thereafter, for a period of 84 days, half of these Ss were offered a high fat diet, whereas the remaining Ss continued to receive wet mash. A series of palatable drinking solutions were also offered. Body weight remained at reduced levels relative to 8 intake controls regardless of the diet offered, even under conditions of high fluid intake generated by the palatable drinking solutions. Results contradict the interpretation of E. J. Mufson and R. S. Wampler (see record 1973-00428-001) that the lower body weight observed in LH-lesioned animals is secondary to lesion-produced "finickiness" and/or dehydration resulting from hypodipsia. Rather, a primary shift in the set point for body weight appears to underlie the reduced levels of weight maintenance in LH-lesioned animals. (16 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Fragmented behavior sequences in rats with lateral hypothalamic lesions: An alternative reason for intrameal prandial drinking.

50 Sprague-Dawley and Long-Evans rats in Stages 3 or 4 after lateral hypothalamic lesions were studied in several feeding situations. As expected, Ss showed intrameal prandial drinking when dry food and water were available. Meals of liquid diet were interrupted by short bouts of activity, and saccharin drinking in Stage 3 was composed of many small drafts. It is suggested that these animals have a propensity to interrupt ongoing behaviors (fragmentation), which can account for general activity and wheel running that occurs along with intrameal prandial drinking. The probability of drinking during meals was decreased with water infusions and increased with NaCl infusion. When they were hungry, recovered laterals ate 4.5 g of dry food without pausing to drink. These new data raise questions concerning the state of the salivary-insufficiency (dry mouth) explanation of intrameal drinking; the fragmentation hypothesis can incorporate the data, and the possible neural correlates of this fragmentation are discussed. (49 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Preoperative sodium experience and hypothalamic lesions in rats.

When a sodium deficit is induced in rats without lesions, they increase their saline intake regardless of prior experience. By contrast, the present experiment with 60 Sprague-Dawley rats found that Ss with lateral hypothalamic lesions increased their saline intake only when they had had preoperative experience ingesting saline in response to a sodium deficit. Ss were given natriuretic and mineralocorticoid treatments to induce sodium appetite. The role of preoperative experience in neural function is discussed. (32 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Gastric pathology and aphagia following lateral hypothalamic lesions in rats: Effects of preoperative weight reduction.

Conducted 2 experiments with a total of 105 male albino rats. In Exp I, body weights of Ss were reduced gradually to 80% of normal weight by restricting food intake (dieting), and then Ss were given lateral hypothalamic (LH) lesions. Compared with Ss of normal body weight sustaining similar brain lesions, the dieted group displayed a shorter period of postoperative aphagia and less gastric pathology. In Exp II, a group of Ss was reduced to 80% of normal body weight by withholding all food (fasting) and then given LH lesions. Compared with dieted Ss sustaining similar brain damage, the fasted group displayed a longer period of postoperative aphagia and greater gastric pathology. Since the duration of aphagia could be shortened or lengthened by simple manipulations of preoperative body weight, the adequacy of sensorimotor or motivational hypotheses to account for aphagia is questioned. Results are more consistent with the suggestion that gastric abnormalities produced by LH lesions inhibit eating. (60 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Continuing gonadal function in rats with ventromedial hypothalamic area lesions.

Gonads of 24 female and 20 male rats with ventromedial hypothalamic (VMH) or sham lesions were examined after 67 days in constant light. Results show that VMH- and sham-lesioned males had normal testes. Sham-lesioned females had small ovaries and no corpora lutea (CL). 7 VMH females had larger ovaries with CL and numerous follicles, 4 had larger ovaries with no CL but numerous follicles, and 4 had ovaries resembling those of sham-lesioned females. Damage was confined to the VMH in females with CL, but it included less or more of the anterior hypothalamus in females lacking CL. Results suggest that since VMH damage permits estrous cycling to continue, the intact VMH acts to inhibit cycling in constant light. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Hyperinsulinemia in rats with ventromedial hypothalamic lesions: Role of hyperphagia.

Examined the relation of hyperinsulinemia to hyperphagia in 18 female hooded Long-Evans rats with lesions of the ventromedial hypothalamus (VMH). Plasma insulin and glucose levels were assayed after a 4-hr fast and 17 min after the initiation of a meal (6 ml of sweetened milk in 7 min) in 8 other Ss with sham lesions, VMH Ss maintained at preoperative body weight by food restriction, and VMH Ss fed ad lib. Both VMH groups displayed basal and postabsorptive hyperinsulinemia compared with the sham-operated group, but insulin levels were greatest under the ad lib feeding condition. It is suggested that VMH hyperinsulinemia is due both to a primary effect of the lesion and to hyperphagia and that marked obesity can result in the absence of basal hyperinsulinemia as a result of hyperphagia with consequent postabsorptive hyperinsulinemia. (14 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)